High-fat diet (HFD) consumption leads to metabolic disorders, gastrointestinal dysfunction and intestinal dysbiosis. Antibiotics also disrupt the composition of intestinal microbiota. The aim of the present study was to investigate the impact of a short-term feeding with HFD on oxidative status, enteric microbiota, intestinal motility and the effects of antibiotics and/or melatonin treatments on diet-induced hepato-intestinal dysfunction and inflammation. Male Sprague–Dawley rats were pair-fed with either standard chow or HFD (45 % fat) and were given tap water or melatonin (4 mg/kg per d) or melatonin plus antibiotics (ABX; neomycin, ampicillin, metronidazole; each 1 g/l) in drinking water for 2 weeks. On the 14th day, colonic motility was measured and the next day intestinal transit was assessed using charcoal propagation. Trunk blood, liver and intestine samples were removed for biochemical and histopathological evaluations, and faeces were collected for microbiota analysis. A 2-week HFD feeding increased blood glucose level and perirenal fat weight, induced low-level hepatic and intestinal inflammation, delayed intestinal transit, led to deterioration of epithelial tight junctions and overgrowth of colonic bacteria. Melatonin intake in HFD-fed rats reduced ileal inflammation, colonic motility and perirenal fat accumulation. ABX abolished increases in fat accumulation and blood glucose, reduced ileal oxidative damage, suppressed HFD-induced overgrowth in colonic bacteria, and reversed HFD-induced delay in intestinal transit; however, hepatic neutrophil accumulation, hepatic injury and dysfunction were further enhanced. In conclusion, the results demonstrate that even a short-term HFD ingestion results in hepato-intestinal inflammatory state and alterations in bacterial populations, which may be worsened with antibiotic intake, but alleviated by melatonin.
The most common microvascular complication of diabetes is diabetic retinopathy (DR). A new and recently emerged marker of oxidative stress and inflammation is monocyte to high-density lipoprotein cholesterol ratio (MHR). Platelet to lymphocyte ratio (PLR) and neutrophil to lymphocyte ratio (NLR) have also been shown as they are biomarkers of systemic inflammation in various diseases. The present study aims to assess MHR, its predictive value and relations between other inflammation markers in DR patients. Materials and Methods: Sixty-eight patients with DR, fifty-four DM patients without DR and forty-two control subjects were included in this study. Complete blood count, lipoprotein and uric acid levels were recorded. MHR was calculated. Results: MHR, NLR and PLR were statistically significantly higher in DR group than DM without DR group (p=0.008, p=0.042, p=0.003, respectively). Then, receiver operating characteristic (ROC) curve analysis was performed and pointed that MHR predicted DR using a cutoff level of 0.0156 with 63% sensitivity and 76% specificity. Conclusion: In this study, we investigated MHR in DR patients and its relationship with other inflammatory markers, lipoproteins and uric acid. We suggested that an elevated admission of MHR may be of benefit to detect DR and to determine the CVD risk of these patients.
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